What it does
Tesamorelin is a 44-amino-acid synthetic analog of human growth hormone-releasing hormone (GHRH). It stimulates pulsatile endogenous GH release from the pituitary, raising IGF-1. Phase 3 trials in HIV-associated lipodystrophy demonstrated reductions in visceral adipose tissue (VAT) of roughly 15–18% and supported the FDA approval of Egrifta in 2010 for that specific indication. Off-label use for non-HIV abdominal adiposity, longevity, or body composition has substantially weaker evidence.
Used for
Dose
- Dose
- 2,000 mcg · once daily
- When
- BedtimeFDA-approved at bedtime in the HIV-lipodystrophy indication for exactly the same reason as the rest of the GHRH axis: GH-pulse alignment during slow-wave sleep.
- How long
- 6 months on / 2 months off
- Site
- subcutaneous
- Food
- fasted
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⚠ Caution
- Active malignancy (relative; raised IGF-1 is theoretically permissive of tumor growth)
- Pituitary surgery, radiation, or trauma — confirm pituitary axis with provider first
- Pregnancy and breastfeeding
- Hypersensitivity to mannitol or other excipients
- Severe respiratory failure or critical illness
- Acute glucose dysregulation; tesamorelin can transiently elevate fasting glucose
Medications & conditions
- Dual GHRH analog stacking — amplified GH/IGF-1 axis activationStacking tesamorelin with another GHRH analog or growth-hormone secretagogue creates redundant mechanism overlap. The combination amplifies endogenous GH release and IGF-1 elevation, increasing the risk of insulin resistance, joint pain, fluid retention, and (theoretically) accelerated growth of any subclinical neoplasm. Use one GH-axis peptide at a time.
- Tesamorelin contraindicated in active oncologyTesamorelin is explicitly contraindicated in patients with active malignancy per the FDA label. GH/IGF-1 axis activation can support tumor growth and is not appropriate during cancer treatment. Discontinue and discuss with the oncology team.
- Tesamorelin with corticosteroid — blunted GH responseUser is taking a corticosteroid. Chronic high-dose glucocorticoid use suppresses the hypothalamic-pituitary axis and meaningfully blunts the GH-releasing effect of tesamorelin. Concurrent use reduces the VAT-reduction benefit documented in Phase 3 trials.
Will it work for me?
Establish a baseline (2–3 readings over 1–2 weeks before starting), then track at consistent intervals.
- Tier 1 — Human RCTIGF-1↑· by 8 weeks; stay within age-adjusted range — do not chase supraphysiologic
- Tier 1 — Human RCTTriglycerides↓· 12–26 weeks
- Tier 1 — Human RCTALT / AST (MASLD context)↓· 12–26 weeksOnly relevant when used in a fatty-liver context with elevated baseline enzymes.
- Tier 2 — Human observationalVisceral adipose tissue (VAT) via DEXA↓· DEXA at 12 and 26 weeksPrimary FDA-trial endpoint — ~15–20% VAT reduction at 26 weeks.
- Tier 3 — Animal / in vitroWaist circumference↓· 12–26 weeksTape-measure proxy for VAT; track alongside DEXA.
Often stacked with
- Ipamorelin — Tesamorelin (GHRH analog, FDA-approved) amplifies the GHRH axis; Ipamorelin adds a selective ghrelin-pathway GH pulse — the same GHRH + GHRP dual-pathway synergy as CJC/Ipamorelin, applied with a more clinically characterised GHRH analog.
Your stack
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